Solar ultraviolet-B radiation and vitamin D: a cross-sectional population-based study using data from the 2007 to 2009 Canadian Health Measures Survey

Climate models predict that in northern middle and high latitudes the expected recovery of stratospheric ozone from the effects of ozone-depleting substances over the coming decades will be substantially augmented by an increase in ozone from climate change [1]. Since stratospheric ozone is a major regulator of solar ultraviolet-B (UV-B) received at the Earth’s surface, this increase in stratospheric ozone implies a decrease in UV-B irradiance. Projected decreases of erythemal UV using the McKinlay-Diffey Erythema action spectrum, which is directly proportional to UV Index, have been estimated between 10 and 15% over the current century [2, 3]. These atmospheric changes may affect human health since solar UV-B exposure is a major source of vitamin D3. Adequate vitamin D levels are necessary to maintain physiologic calcium and phosphorous for normal bone mineralization and to prevent rickets, osteomalacia and osteoporosis [4]. Vitamin D has also been associated with a decreased risk of infections, cancers, diabetes, cardiovascular disease, and autoimmune diseases [5].

Vitamin D in meaningful amounts is naturally available in only a few foods, such as fatty fish, in addition to fortified milk and supplements [5]. Vitamin D3 is synthesized endogenously in human skin following exposure to UV-B (280–315 nm) radiation in sunlight, which spontaneously photoisomerizes 7-dehydrocholesterol to pre-vitamin D3 [6, 7]. Pre-vitamin D3 is subsequently converted to vitamin D3 by thermal isomerisation, which then enters the circulation and is hydroxylated in the liver to long-lived 25-hydroxyvitamin D (25(OH)D3). 25(OH)D is the main indicator of total vitamin D status and represents the sum of vitamin D from both cutaneous synthesis and dietary intake [8].

Since foods are naturally low in vitamin D, the prevalence of vitamin D insufficiency in some populations is thought to result from inadequate exposure to sunlight [8]. The solar zenith angle, which varies by latitude, season and time of day, determines the amount of absorption and scattering of solar UV-B radiation and thus the intensity of sunlight at ground-level [9]. Stratospheric ozone and other constituents with absorption features in the UV-B region, clouds, aerosols, surface reflectivity (albedo), and altitude, also affect the amount of solar UV-B reaching the ground [9, 10]. The association between solar UV-B and vitamin D is not straightforward, since living in a sunny climate does not ensure sufficient vitamin D status [11, 12]. Vitamin D availability also depends on personal and lifestyle factors including skin pigmentation (increased melanin in darker skin naturally blocks cutaneous synthesis of vitamin D3) [13], age (the amount of 7-dehydrocholesterol in the skin decreases with age) [14], dietary and supplemental intake [15], adiposity (storage of vitamin D in adipose tissue decreases its bioavailability) [16], and sunlight exposure (when and how long unprotected skin is exposed) [17].

In Canada, there is a high prevalence of low vitamin D status, particularly in the winter [18–20]. Above 42°N exposure to sunlight during the winter months is not sufficient to initiate cutaneous production of vitamin D3 [21, 22]. Approximately 26% of the Canadian population has 25(OH)D concentrations that are inadequate for bone health (< 50 nmol/L) [23]. Recent studies in Canada have examined differences in vitamin D status by sex, age, ethnicity, body mass index (BMI), dietary intake, and vitamin D supplementation [23–28]. However, these epidemiologic studies used season, latitude, or time outdoors as proxy measures for solar UV-B exposure. Thus it was not possible to determine the extent to which projected decreases in solar UV-B radiation may impact on 25(OH)D concentrations at the population level. The primary objective of this study was to quantify the association between ground-level solar UV-B irradiance and serum 25(OH)D concentrations in the Canadian population and to examine factors that modify this relationship.

We used a secondary analysis of data from the 2007 to 2009 CHMS to examine the association between serum concentrations of 25(OH)D and ground-level solar UV-B. This is the first study in Canada to quantify the association between ambient solar UV-B and 25(OH)D in a nationally representative sample. The comprehensiveness of the CHMS made it possible to adjust for personal and lifestyle factors that influence vitamin D status and to examine effect modification. There is currently no standardized method to assess sunlight exposure to explain variation in vitamin D status. The time period over which solar UV-B exposure is measured varies markedly across studies, from one week up to one year. In our study, 25(OH)D levels measured on a given date were influenced the most by the cumulative effect of ambient solar UV-B radiation over the 91-days prior to blood draw. The most relevant time period for solar UV-B exposure with respect to 25(OH)D has not been addressed in previous studies. Unadjusted for other factors, season was a relatively good proxy for 91-day UV-B compared to latitude. Significant differences in 25(OH)D were evident only between the summer (July to September) and winter (January to March) and between high (49–54°N) and medium (45–47°N) latitudes. However, geographic heterogeneity across the CHMS sites may be too small to capture the effect of latitude. Additionally, it is difficult to separate season and latitude effects due to the sampling design of the CHMS.

In a recent study from the Women’s Health Initiative Calcium plus Vitamin D Clinical Trial, mean annual regional solar irradiance at the location of residence accounted for 1% of the total variability in 25(OH)D, whereas month of blood draw accounted for 3% [37]. Compared to our results, this suggests that the one year period over which solar irradiance was averaged was too long to accurately capture the effect of solar UV-B exposure. Another population-based study used data from the Adventist Health Study-2 to examine erythemal zone (average monthly noon erythemal radiation at the location of residence) during the two months prior to blood collection, UV season (categorized into three groups according to erythemal zone), season, and latitude as predictors of 25(OH)D [38]. In multivariable analysis, UV season and erythemal zone were more strongly associated with 25(OH)D than season and latitude, demonstrating that measures of solar UV irradiance, as opposed to season and latitude as proxies, are better predictors of 25(OH)D. Our results demonstrate that future epidemiologic studies should assess solar UV-B exposure over a three month period to best capture the variability in 25(OH)D concentrations.

Similar to our results, the population-based Canadian Multicentre Osteoporosis Study identified fall and winter season, BMI ≥ 30 kg/m², darker skin pigmentation, and lower vitamin D supplementation as the strongest predictors of decreased 25(OH)D among Canadians over 35 years of age across seven cities [25]. Age was not found to be a significant independent predictor of 25(OH)D; however, most study participants were older than 51 years of age. Regular participation in physical activity was a significant predictor for females only. There was a significant interaction between vitamin D supplementation and season, which was not found in our study; although, the dose of vitamin D supplementation for respondents to the CHMS was not measured. In our study, we found that age and PAI were significant effect modifiers of the relationship between 91-day UV-B and 25(OH)D. The interaction with age may reflect that synthesis of vitamin D3 decreases with increasing age due to reduced concentrations of 7-dehydrocholesterol in the skin as well as alterations in skin morphology [14]. Although the association between 91-day UV-B and 25(OH)D was strongest within the youngest age group, the oldest age group had the highest levels of 25(OH)D. This may suggest that dietary and supplemental intake of vitamin D play an important role in achieving adequate levels of 25(OH)D among older individuals. The interaction with PAI may suggest that physical activity is a good proxy for time spent outdoors in the sun. This is consistent with results from the Third National Health and Nutrition Examination Survey, in which regular outdoor physical activity, as opposed to intense indoor physical activity, was associated with higher levels of 25(OH)D [39].

We estimate that a 10 to 15% decrease in solar erythemal UV projected over the current century [2, 3] corresponding to a decrease in solar UV-B irradiance of less than 2 kJ/m² in Canada, would be associated with less than a 1 nmol/L decrease in mean 25(OH)D for the population. Although solar UV-B irradiance is significantly associated with 25(OH)D concentrations, the small magnitude of effect may be due to inadequate sun exposure at the individual level as a result of behaviour and/or the “vitamin D winter” that is characteristic of high latitudes. Public health messages should increase awareness about practising safe sun exposure optimal for vitamin D3 synthesis during the summer in addition to promoting dietary and supplemental intake of vitamin D and proper nutrition and physical activity to maintain a healthy body weight. Vitamin D reference intakes should be set at levels high enough to prevent vitamin D insufficiency among individuals who do not obtain adequate solar UV-B exposure.

The main strengths of our study include its large sample size, which was representative of the Canadian population, and the low frequency of missing data. In contrast to most epidemiologic studies, we did not use season or latitude as a proxy for solar UV-B exposure, and we were able to examine personal and lifestyle factors that influence vitamin D status. A limitation of our study is the low response rate for blood draw among the CHMS respondents. Measurement error associated with solar UV-B irradiance, serum 25(OH)D concentrations, and other predictors likely contribute to the low variability in 25(OH)D captured in the multivariable regression model. Solar UV-B irradiances were calculated for clear-sky conditions because of the highly variable and unpredictable effect of clouds on solar UV-B irradiance [9]. The ECMWF cloud field does not contain cloud base and cloud top heights, which are required in the TUV model. The adjustment for background aerosols did not account for highly polluted regions, which may reduce ground-level solar UV-B due to scattering and absorption [9]. Lastly, solar UV-B irradiances calculated using the TUV model were not weighted for the vitamin D action spectrum, which corresponds to the conversion of 7-dehydrocholesterol to pre-vitamin D3. Limitations of the CHMS data include a lack of assessment of percent fat, skin pigmentation, the duration or timing of recent sun exposure, sunscreen use in all participants, typical clothing coverage outdoors, recent travel to a sunny climate, and the frequency or dose of vitamin D supplementation. Despite these limitations, our results are comparable to recent predictive models that explained 21 to 42% of the total variability in 25(OH)D [37, 38, 40–42]. Additional factors not accounted for, such as genetic differences in vitamin D related genes, may play an important role in determining 25(OH)D concentrations [43, 44]. It is likely that many factors each impart a small but significant influence on the vitamin D status of human populations.

Solar UV-B irradiance explains a small but statistically significant proportion of the total variability in 25(OH)D concentrations. Future climate change and ozone recovery is expected to have a small effect on mean serum 25(OH)D for the Canadian population, at latitudes 43–54°N, suggesting that public health messages and interventions to promote sufficient vitamin D status should target behavioural factors including safe sun exposure with sunscreen use, enhanced dietary and supplemental intake of vitamin D and maintenance of a healthy body weight. These results likely pertain to other populations in developed countries at similar latitudes. Future investigations using longitudinal studies and observations of UV-B irradiance are needed to better evaluate the causal relationship between ambient solar UV-B and vitamin D status in humans.